Supporting data for “The Function of LEM-3 Endonuclease in Regulating Cell Fate Determination”

This project studies the effects of LEM-3 on cell fate determination in the nematode Caenorhabditis elegans. The study was mostly performed in the touch receptor neurons (TRNs) of C.elegans. There are six TRNs in C.elegans, including ALML, ALMR, PLML, PLMR, AVM, and PVM. We knocked out the lem-3 gene in C. elegans, labeled various neurons with fluorescent proteins driven by specific gene promoters, and observed the effects of lem-3 knockout on neuronal cell fate. We also used various biochemical methods to manipulate biological processes in C. elegans, such as using drugs to regulate the activity of topoisomerases to block the DNA replication process. One feature of the cell fate change caused by abnormal lem-3 is that its absence causes the formation of intercellular channels between neurons and sister neurons. We evaluated the degree to which cell fate was affected in different situations by quantifying the penetrance of intercellular canals.

Figure 3C, 3D, 12C, 14B, 21: penetrance of intercellular canals in different neuronal subtypes; Figure 7E: percentage of independent and mixed transcription of genes in different types of syncytia; Figure 9B: length of intercellular canals at different time points during C.elegans development; Figure 10B, 10C: intensity of fluorescent signals in different neuronal subtypes; Figure 12B: percentage of nuclear membrane connections in syncytia; Figure 15C: penetrance of intercellular canals in AVM neurons under different experimental conditions. Figure 16A: percentage of different syncytia types; Figure 17E: Ratio of different cell fate-affecting outcomes.